Tendon injuries through overuse, overload and/or tears are common conditions which can dramatically alter joint mechanics in a complex and multifactorial manner leading to significant joint damage. This joint damage can be manifested as articular cartilage degeneration, injury to adjacent (intact) tendons, and abnormal joint kinematics and kinetics. Unfortunately, the mechanism by which tendon injuries lead to permanent joint damage remains unclear and as a result, clinicians offer advice without scientific understanding of the deleterious effects on the uninjured tendons and adjacent joint tissues. The in vivo cause and effect relationships that these mechanical alterations and disruptions have on the associated structures cannot be evaluated in tissue culture or human cadaveric studies and therefore remains unknown. Although clinical studies have established a relationship between even a single joint injury event and the development of deleterious changes in the affected joints that can be transient or permanent, the mechanism by which these changes occur remains unclear. Recently, we extended our established in vivo rat model of supraspinatus tendon tears to include tears of other rotator cuff tendons which results in changes in joint kinematics and kinetics, adjacent (intact) rotator cuff tendons, as well as the long-head of the biceps tendon providing a direct parallel to the changes observed in the human condition. With the development of this novel model and in coordination with our previously established rotator cuff tendon overuse model, the overall objective of this study is to elucidate the mechanisms governing the relationship between tendon injury and joint damage in common clinical conditions. By providing a well-defined mechanical milieu, our global hypothesis is that increasing joint damage (measured by changes in adjacent (intact) tendons, articular cartilage, and joint kinematics and kinetics) will be explained through two mechanically-based mechanisms: 1) tendon overload/overuse and 2) tendon force couple disruption (joint balance). Our Specific Aims are: Specific Aim 1: Determine if the mechanism of overload (1a) or overuse (1b) leads to joint damage in the absence of force couple disruption and Specific Aim 2: Determine if the mechanism of force couple disruption leads to joint damage. This study is innovative in that it defines the contributory roles of common mechanical injury mechanisms (overload, overuse and force couple disruption) through a novel extension of an established in vivo animal model that mimics the human condition and further, evaluates joint damage in a multidisciplinary manner including a novel ambulation assessment method where joint kinematics and kinetics can be rigorously quantified in vivo. Results of this study will not only define the in vivo mechanical processes which cause joint damage due to tendon injury, but will also provide a framework and model system in which physicians could better advise patients on outcomes and in which targeted treatment modalities could be evaluated in a controlled manner in order to guide physicians on an optimal treatment strategy long-term for common injuries.